Moreover, infection with CagA-positive H pylori strains in atherosclerotic stroke patients is associated with greater IMT and poorer short-term outcomes than those of CagA-negative patients.[49] The levels of CRP, a sensitive marker for the detection of a systemic inflammatory response, trended toward higher levels in CagA-positive patients than those in CagA-negative patients.[50] Molecular mimicry between CagA and proteins presented in the wall of medium- and large-sized arteries is one proposed mechanism for the initiation and development of atherosclerosis by H pylori infection.[51]. The gene discussed is S100A8; the disease is infection.